4-(3,4-Dimethoxyphenyl)butyl azide | 583825-39-2

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 4-(3,4-Dimethoxyphenyl)butyl azide
• 英文别名: 4-(4-azidobutyl)-1,2-dimethoxybenzene
• CAS: 583825-39-2
• 化学式: C₁₂H₁₇N₃O₂
• 分子量: 235.286
• InChiKey: RNVFMLLRXORVME-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.3
• 重原子数：
  17
• 可旋转键数：
  7
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.5
• 拓扑面积：
  32.8
• 氢给体数：
  0
• 氢受体数：
  4

反应信息

• 作为反应物：
  描述：

  4-(3,4-Dimethoxyphenyl)butyl azide 在 lithium aluminium tetrahydride 作用下， 以 四氢呋喃 为溶剂， 生成 4-(3,4-Dihydroxyphenyl)butyl amine hydrobromide
  参考文献：
  名称：

  Sodium channel blockers

  摘要：

  本发明涉及钠通道阻滞剂。本发明还涉及使用这些钠通道阻滞剂进行治疗的各种方法。

  公开号：

  US20030195160A1
• 作为产物：
  描述：

  4-(3,4-二甲氧苯基)丁酸 以 四氢呋喃 为溶剂， 生成 4-(3,4-Dimethoxyphenyl)butyl azide
  参考文献：
  名称：

  Sodium channel blockers

  摘要：

  本发明涉及钠通道阻滞剂。本发明还涉及使用这些钠通道阻滞剂进行治疗的各种方法。

  公开号：

  US20030195160A1

文献信息

• Enantioselective intramolecular C–H amination of aliphatic azides by dual ruthenium and phosphine catalysis
  作者：Jie Qin、Zijun Zhou、Tianjiao Cui、Marcel Hemming、Eric Meggers

  DOI：10.1039/c9sc00054b

  日期：——

  organic azide to form an intermediate iminophosphorane and transfers the nitrene unit to the ruthenium providing an imido ruthenium intermediate which engages in the highly stereocontrolled C–H amination. This dual catalysis combines ruthenium catalysis with the Staudinger reaction and provides a novel strategy for catalyzing enantioselective C–H aminations of unactivated aliphatic azides.

  脂肪族叠氮化物的催化对映选择性分子内C（sp 3）-H胺化反应是构建手性饱和环胺的有效方法，该手性饱和环胺构成生物活性化合物中的重要结构基序。我们报告了一个双催化体系，涉及手性金属双（吡啶基-NHC）钌配合物和三（4-氟苯基）膦（均为1 mol％），这有助于将脂族叠氮化物环化为手性α-芳基吡咯烷高达99％ee的对映选择性，包​​括可以转化为抗肿瘤生物碱的吡咯烷（R）-（+）-crispine。从机理上讲，膦可活化有机叠氮化物以形成中间体亚氨基正膦，并将腈单元转移至钌，从而提供亚胺基钌中间体，该中间体可参与高度立体控制的CH氨基化反应。这种双重催化将钌催化与Staudinger反应结合在一起，为催化未活化脂肪族叠氮化物的对映选择性C–H胺化提供了一种新的策略。
• Methods of using phenolic guanidine sodium channel blockers
  申请人：PARION SCIENCES, Inc.

  公开号：US20040198744A1

  公开（公告）日：2004-10-07

  The present invention relates to sodium channel blockers. The present invention also relates to a variety of methods of treatment using these sodium channel blockers.

  本发明涉及钠通道阻滞剂。本发明还涉及使用这些钠通道阻滞剂的各种治疗方法。
• Phenolic guanidine sodium channel blockers
  申请人：PARION SCIENCES, Inc.

  公开号：US20040204424A1

  公开（公告）日：2004-10-14

  The present invention relates to sodium channel blockers. The present invention also relates to a variety of methods of treatment using these sodium channel blockers.

  本发明涉及钠通道阻滞剂。本发明还涉及使用这些钠通道阻滞剂的各种治疗方法。
• Design, Synthesis, and Structure−Activity Relationships of Novel 2-Substituted Pyrazinoylguanidine Epithelial Sodium Channel Blockers:  Drugs for Cystic Fibrosis and Chronic Bronchitis
  作者：Andrew J. Hirsh、Bruce F. Molino、Jianzhong Zhang、Nadezhda Astakhova、William B. Geiss、Bruce J. Sargent、Brian D. Swenson、Alexander Usyatinsky、Michael J. Wyle、Richard C. Boucher、Rick T. Smith、Andra Zamurs、M. Ross Johnson

  DOI：10.1021/jm051134w

  日期：2006.7.1

  Amiloride (1), the prototypical epithelial sodium channel (ENaC) blocker, has been administered with limited success as aerosol therapy for improving pulmonary function in patients with the genetic disorder cystic fibrosis. This study was conducted to synthesize and identify more potent, less reversible ENaC blockers, targeted for aerosol therapy and possessing minimal systemic renal activity. A series of novel 2-substituted acylguanidine analogues of amiloride were synthesized and evaluated for potency and reversibility on bronchial ENaC. All compounds tested were more potent and less reversible at blocking sodium-dependent shortcircuit current than amiloride. Compounds 30-34 showed the greatest potency on ENaC with IC50 values below 10 nM. A regioselective difference in potency was found (compounds 30, 39, and 40), whereas no stereospecific (compounds 33, 34) difference in potency on ENaC was displayed. Lead compound 32 was 102-fold more potent and 5-fold less reversible than amiloride and displayed the lowest IC50 value ever reported for an ENaC blocker.
• SODIUM CHANNEL BLOCKERS
  申请人：Johnson, Michael R.

  公开号：EP1485359A2

  公开（公告）日：2004-12-15